AbstractProtein kinase C (PKC) is a family of enzymes detected in a diverse range of cell types where they regulate various cellular functions such as proliferation, differentiation, cytoskeletal remodelling, cytokine production, and receptor‐mediated signal transduction. In this study we have analyzed the expression of 11 PKC isoforms (‐α, ‐βI, ‐βII, ‐γ, ‐δ, ‐η, ‐θ, ‐ε, ‐ζ, ‐ι/λ, and ‐µ) in osteoblasts from patients with osteoarthritis (OA) and rheumatoid arthritis (RA) in comparison with osteoblasts from post‐traumatic (PT) patients. By Western blotting analysis, nine isoforms, ‐α, ‐βI, ‐βII, ‐δ, ‐θ, ‐ ε, ‐ζ, ‐ ι/λ, and ‐µ, were detected in osteoblasts. In RA and OA patients, PKC ‐θ and ‐µ were greater expressed whereas PKC‐ε and ‐ζ decreased when compared with normal cells. The subcellular distribution and quantitative differences were confirmed by immuno‐electron microscopy. Furthermore, we demonstrated that treatment with the proinflammatory cytokines, IL‐1β and TNF‐α, significantly decreased PKC‐ζ expression in PT osteoblasts. This suggests that proinflammatory cytokines can modulate the expression of this PKC isoform in osteoblasts in a way which is similar to changes detected in arthritic patients. J. Cell. Biochem. 103: 547–555, 2008. © 2007 Wiley‐Liss, Inc.